Polish journal of occupational medicine and environmental health最新文献

Mutagenicity and toxicity of urine samples of 30 coke oven workers (group I) and 26 individuals composing a control group (group II) was estimated using Ames test with Salmonella typhimurium strains TA 98 and TA 100. Urine mutagenicity and toxicity, tested with strain TA 98 and metabolic activation, was significantly higher in group I than in group II. Using the strain TA 100, urine samples of coke oven workers showed only direct toxicity. Mutagenic and toxic activity was observed mostly in workers exposed to the highest BaP concentrations. No correlation was found between obtained results and tobacco smoking. Increased urinary mutagenic activity in group I resulted from exposure to very high BaP concentrations. It is concluded that urine samples of exposed coke oven workers should be periodically tested for mutagenic activity. Workers with mutagenic urine ought to be shifted to work posts with lower exposure to mutagens.

An oral dose of 6.2 mmoles of diachloromethane (DCM), bromochloromethane (BCM) or dibromomethane (DBM) per kg body mass yielded a maximum carboxyhemoglobin (COHb) level of about 9% (at 6 hr), 11% (at 8 hr) and 22% (at 12 hr), respectively. Pretreatment of rats with isoniazid, 4 x 0.36 mmol/kg i.p., produced significant enhancements of the COHb formation; the values were 18.0 +/- 0.8% COHb after DCM, 24.1 +/- 0.8% COHb after BCM, and 39.0 +/- 1.3% COHb after DBM. Prior administration of phenobarbital, 4 x 0.31 mmol/kg i.p., caused no appreciable alterations in the COHb levels after DCM and slight but significant increases after BCM as well as after DBM. The data indicate that the oxidative metabolism of dihalomethanes to carbon monoxide is mainly catalyzed by cytochrome P-450 IIE1 and that the DCM-evoked COHb formation seems to be a method of testing whether a chemical is an inducer of this form of cytochrome P-450 in vivo.

In all of 11 observed patients with bakers' asthma, coughing preceded the development of dyspnea. Seventeen coughing atopic patients working in a bakery were observed for 2 years and treated with ketotifen and disodium cromoglycate (DSCG). Four of the patients developed asthma. Ketotifen prevented coughing attacks but did not prevent asthma development. Bronchodilators interrupted cough attacks. DSCG was ineffective.

Three short-term tests were used for evaluation of the genotoxic activity of four surface active agents. These were: Ames, Salmonella reversion assay using 4 tester strains (TA97a, TA98, TA100 and TA102), the micronucleus test int the bone marrow of Balb C mice and in vivo sister chromatid exchange (SCE) analysis in SFIS or Balb C mice. The frequency of micronucleated PCEs did not exceed the control values in mice of both sexes after intraperitoneal administration of all four compounds. Three preparations--Sulfosuccinate IO-5, Rokamid MRZ 17 and Rokacet RZG7P2 produced a negative response in Salmonella strains gene mutation assay and SCE induction test in mouse bone marrow cells. The Roksol TL-7 induced frameshift and base-pair substitution mutations in Salmonella tester strains both with and without S9 (prepared from the liver of rats which had been pretreated with Aroclor 1254). Evidently positive results (more than a twofold increase in the number of revertants per plate) were observed in tester strain S. typhimurium TA97a (with and without S9 metabolic activation) and S. typhimurium TA100 (with S9 metabolic activation) at a dose of 0.2 microliter Roksol TL-7 per plate. Roksol TL-7 caused slight increase in the SCE level in mouse bone marrow cells. A significant increase in SCE frequency was observed at doses of 50, 75 and 100 mg/kg.

Spontaneous locomotor activity in rotating wheels was investigated in rats exposed repeatedly (i.p. daily injections, five days a week for two weeks) to an agricultural organophosphorus pesticide, chlorphenvinphos (CVP) at doses of 1.0 and 3.0 mg/kg. After a seven day interval each rat was injected with a single 3.0 mg/kg test dose of CVP in order to assess the stability of tolerance. Concomitant changes in blood and the brain ChE activity were also investigated. It was found that exposure to CVP at a low dose (1.0 mg/kg), resulting in less than 50% reduction of ChE activity in blood and in the brain, did not produce changes in spontaneous locomotion in rotating wheels in the rat. Higher doses (3.0 mg/kg) inhibited blood and the brain ChE by more than 50% and reduced locomotion. Under conditions of repeated exposure to CVP at the symptomatic (3.0 mg/kg) dose ChE activity remained low throughout the exposure period, however, locomotor activity returned to a normal level, i.e. tolerance developed, within less than five days. Seven days after termination of the repeated exposure, the behavioral subsensitivity to CVP still remained. The biochemical data suggest that it may be related, at least partially, to a diminished vulnerability of ChE in some parts of the brain to CVP induced inhibition.

In the group of 37 patients with chronic carbon disulphide (CS2) intoxication manifested by encephalopathy, polyneuropathy or psycho-organic syndrome and complaining for vertigo, a statokinesiometric test was performed with open and closed eyes, and with visual stimulation. Basic test parameters of stabilograms and statokinesiograms were compared with standard values of the control group. Results of the test were additionally verified by electronystagmography with the recording of spontaneous, positional, optokinetic and post-rotatory nystagmus as well as the eye-tracking test. The statokinesiometry revealed postural stability disorder in 72.9% of patients. Balance disorders detected by means of this test showed high compatibility with results of electronystagmography which confirmed damage of the central part of vestibular system due to CS2 intoxication.

The development of semiconductor production has been accompanied by an increased use of toxic production materials and an increased release of potential toxic wastes, which are harmful to health and environment. This paper gives an overview of occupational health hazards resulting from production materials in the microelectronics industry and from waste products originating as gases from plasma etching processes in photolithography during semiconductor production. The paper proposes methods for using experimental toxicology to investigate the occupational risks from complex mixtures of chemicals in the semiconductor industry.

Recent advances in molecular biology and toxicology have greatly contributed to the early diagnosis of biological changes which may evoke neoplasms. This paper reviews the issues regarding the screening of persons occupationally exposed to carcinogenic aromatic amines. The screening was designed for an early detection of bladder cancer by means of biochemical tests. The applied tests facilitated the estimation of the level of aromatic amines which penetrate an organism (biomarkers of exposure), early diagnosis of the biochemical disorders which may influence cancer development (biomarkers of early effects) and the detection of genetic predispositions which enhance risk of such disorders (biomarkers of susceptibility).

The majority of investment in manufacturing industries in the newly industrialized countries come from foreign companies or investors. This vital source of new jobs and capital for the development of infrastructure brings with it some very significant longterm costs in environmental remediation and workers' compensation insurance that are seldom discussed with candor. These costs may be considered a necessary step on the road to industrialization by many developing countries. But the longterm costs may be high enough to sustain the relative poverty of the country. Moreover, the absence of value added in the process of manufacturing may insure the continued economic dependence on foreign interests. The inadequacy of international environmental law is of concern to a few important organizations. But the extent of environmental degradation in many newly industrialized countries warrants far more effort at regulation and enforcement. Likewise, the high levels of worker fatalities and injuries in developing countries remind us of the need for international cooperation and health and safety program development.

Environmental pollutants seem to be responsible for dramatical increase of allergic disorders that have been observed lately. The best documented environmental factors facilitating allergy development are: ozone, diesel-exhaust particulate matter and tobacco smoke. Formaldehyde and SO2 seem to be also very important but still are not sufficiently documented. Mechanisms involved in allergy promotion include: better penetration of allergens across respiratory mucosa or direct modulation of immunological response.